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Qaidam cattle are a typical Chinese native breed inhabiting northwest China. They bear the characteristics of high cold and roughage tolerance, low‐oxygen adaptability and good meat quality. To analyze the genetic diversity of Qaidam cattle, 60 samples were sequenced using whole‐genome resequencing technology, along with 192 published sets of whole‐genome sequencing data of Indian indicine cattle, Chinese indicine cattle, North Chinese cattle breeds, East Asian taurine cattle, Eurasian taurine cattle and European taurine cattle as controls. It was found that Qaidam cattle have rich genetic diversity in Bos taurus, but the degree of inbreeding is also high, which needs further protection. The phylogenetic analysis, principal component analysis and ancestral component analysis showed that Qaidam cattle mainly originated from East Asian taurine cattle. Qaidam cattle had a closer genetic relationship with the North Chinese cattle breeds and the least differentiation from Mongolian cattle. Annotating the selection signals obtained by composite likelihood ratio, nucleotide diversity analysis, integrated haplotype score, genetic differentiation index, genetic diversity ratio and cross‐population extended haplotype homozygosity methods, several genes associated with immunity, reproduction, meat, milk, growth and adaptation showed strong selection signals. In general, this study provides genetic evidence for understanding the germplasm characteristics of Qaidam cattle. At the same time, it lays a foundation for the scientific and reasonable protection and utilization of genetic resources of Chinese local cattle breeds, which has great theoretical and practical significance. [ABSTRACT FROM AUTHOR]

A method for coupling MODFLOW/MT3DMS for the simulation of variable-density ground water flow is described. Results show that the MODFLOW/MT3DMS approach gives accurate solutions for problems involving variable-density ground water flow on solute transport.

Introduction The behaviors of solutes in porous media over a variety of spatial and temporal scales are generally assessed with the help of analytical or numerical solutions. STANMOD (STudio of [...]

Abstract Background This study was conducted to investigate the expression of CXCR4 in portal vein tumor thrombus (PVTT) tissue and its possible role in the invasiveness of tumor thrombus cells. Methods We detected differential expression of CXCR4 between PVTT and hepatocellular carcinoma (HCC) by an immunohistochemical assay. Lentivirus-mediated RNA interference and a migration assay were performed on human primary cells derived from PVTT to study the impact of CXCR4 on the invasiveness of HCC. Results The expression of CXCR4 in tumor thrombus tissue was higher than that in HCC tissue. The invasion ratio of PVTT cells was significantly decreased (P < 0.05) after being infected with a CXCR4-targeting siRNA lentivirus, indicating that downregulation of CXCR4 by lentivirus-mediated RNA interference significantly impaired the invasive potential of PVTT. Conclusions These results indicate that CXCR4 is an effective curative target for hepatocellular carcinomas with PVTT.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Here, we identified that increased miR‐23a expression in HCC tissues was associated with worse survival. More importantly, we found that STAT5A was a target of miR‐23a, whose levels significantly decreased in tumor tissues. Stable expression of STAT5A in Huh7 cells suppressed glucose metabolism and tumor growth. Finally, this study showed that increased miR‐23a negatively regulated STAT5A, which further activated AKT signaling to enable rapid metabolism for accelerated tumor growth in HCC. Taken together, our results demonstrated that the miR‐23a‐STAT5A‐AKT signaling pathway is critical to alter glucose metabolism in HCC and may offer new opportunities for effective therapy. [ABSTRACT FROM AUTHOR]

Background: Vascular invasion, including microvascular invasion (MVI) and portal vein tumor thrombus (PVTT), is associated with the postoperative recurrence of hepatocellular carcinoma (HCC). We aimed to investigate the potential impact of hepatitis B virus (HBV) activity on the development of vascular invasion.Methods: Patients with HBV and tumor-related factors of HCC who had undergone hepatectomy were retrospectively enrolled and analyzed to identify the risk factors for developing vascular invasion.Results: A total of 486 patients were included in this study. The overall proportion of patients with vascular invasion, including MVI and PVTT, was 60.3% (293/486). The incidence of MVI was 58.2% (283/486) whereas PVTT was 22.2% (108/486). Univariate analysis revealed that positive Hepatitis B virus surface Antigen (HBsAg) was significantly associated with the presence of vascular invasion. In a multivariate regression analysis carried out in patients with HBV-related HCC, positive Hepatitis B virus e Antigen (HBeAg)(OR = 1.83, P = 0.019) and a detectable seral HBV DNA load (OR = 1.68, P = 0.027) were independent risk factors of vascular invasion. The patients in the severe MVI group had a significantly higher rate of positive seral HBsAg (P = 0.005), positive seral HBeAg (P = 0.016), a detectable seral HBV DNA load (> 50 IU/ml) (P < 0.001) and a lower rate of anti-viral treatment (P = 0.002) compared with those in the mild MVI group and MVI-negative group. Whereas, HCC with PVTT invading the main trunk showed a significantly higher rate of positive HBsAg (P = 0.007), positive HBeAg (P = 0.04), cirrhosis (P = 0.005) and a lower rate of receiving antiviral treatment (P = 0.009) compared with patients with no PVTT or PVTT invading the ipsilateral portal vein. Patients with vascular invasion also had a significantly higher level of seral HBV DNA load than patients without vascular invasion (P = 0.008).Conclusions: In HCC patients, HBV infection and active HBV replication were associated with the development of vascular invasion. [ABSTRACT FROM AUTHOR]